Heme metabolism and its relationship to the non-pathological transient porphyria in the fetus and newborn will be pursued. The major purpose of this proposal will be to determine the biochemical basis for the accumulation of porphyrin metabolites during fetal development. This will necessitate the identification of the major porphyrin metabolite accumulating during development and a thorough exploration of the possible regulatory or control mechanisms unique to the fetus. The ontogeny of control mechanisms will be compared in adult, newborn, and fetal animals. Establishment of whether the type of porphyrin metabolite seen during this transient period of time is initially formed in primary liver parenchyma cells or in erythropoietic tissue will be required. The isolation and characterization of delta- aminolevulinic acid synthetase of fetal and adult origin is critical to the understanding of regulatory mechanisms. As critical may be the effect of external agents as regulatory substance on the control of heme.